Examination of Witnesses (Questions 20-39)
DR PETER
NASH, MR
PETER SOUL
AND DR
MANDY BAILEY
WEDNESDAY 22 MAY 2002
20. Does that give an indication that further
research work needs to be done in this area? I know it is a Department
of Health issue.
(Dr Bailey) It is a Department of Health issue, yes.
21. What is your understanding of it?
(Dr Bailey) I am afraid I do not know whether or not
the Department of Health are funding any work in this particular
area.
22. You told us earlier on that there was a
whole range of research work going on, and that you were happy
to fund research provided you found there was some benefit. Can
you just outline what the main threads of the research are that
the Department is funding?
(Dr Bailey) Yes. The DEFRA research programme is divided
into four main areas. There is some overlap between them, but
we are doing quite a lot of work in relation to the epidemiology
of the disease. We are also looking at transmission of the disease.
(When I say "the disease", I really should say two diseases,
BSE and scrapie, because we are funding both work on BSE and on
scrapie.) We also have quite a large programme on diagnostic developments,
because clearly that is a key area. There is pathogenesis, that
is, looking at the development of the disease in the animal. The
work on pathogenesis has been incredibly important in determining
which tissues in the animal become infected and at what stages
they become infected. That has been the basis of most of the control
measures that have been put in place both within the UK and within
Europe.
23. One of the popular myths from the Daily
Mail is that intensive farming really is the cause of all
health problems. Does any of the work that you have just outlined
overlap with that?
(Dr Bailey) The work that I have just described to
you is the work that is funded in the TSE area by the Department,
and clearly that does not represent the whole of DEFRA's research
programme. I am afraid I do not have information on the rest of
DEFRA's research programme. If you wish to have further information
on that, we would need to provide you with some written comments.
24. It would be very helpful if you could write
to us on that, because one of the urban myths at the moment is
that intensive farming by definition leads to disease, and I have
heard it said that intensive farming has led to BSE. There may
not be any proof of that at all, but it would be very helpful
if you could outline whether any of the work the Department funds
looks at that.
(Dr Nash) There is a sort of connection, an indirect
connection, in the link with BSE and the consumption of meat and
bonemeal. For example, there has been a much higher prevalence
in the dairy cattle that are more intensively fed than beef cattle,
but it is not a necessary connection, of course, because we have
been able to do something about it. Nevertheless, there is a sort
of link there.
Chairman
25. You said earlier that you were quite happy
to examine heretical views—you did not use that phrase—that
if people were coming at it from a different angle, you were interested
in exploring those views because we did not have the definitive
solution and there was just the odd chance that this stray particle
might split the atom, as it were. I have had a meeting with Professor
Ebringer, and I do not pretend that I understand the science expertly.
I mentioned earlier on that his contention is that BSE is caused
by an auto-immune response to the common orgasm Acinetobacter,
it cannot be transmitted to humans, and he is trying to develop
a diagnostic test for BSE in live animals. You said you had looked
at this and decided it was not possible to pursue that because
it seriously challenged the prion hypothesis. What was the basis
of that conclusion?
(Dr Bailey) There were a number of reasons. Part of
what Professor Ebringer said is to do with the fact that if you
inject brain material into animals from brains that are not suffering
from BSE, you can get a neurological disorder, and this is to
do with an immune response, but in fact, the pathology of the
disease, what it looks like when you look at the brains, is totally
different from TSE. That was one of their reasons. I suppose the
most compelling reason is that Professor Ebringer's theory is
based on the fact that there has to be an immune response, and
there has been some scientific work done in mice where the immune
response has been destroyed, and you can still transmit TSEs to
mice who have no immune system, which means that you do not need
an immune system for the transmission of TSEs, and therefore it
does not support the hypothesis that what is happening is that
the immune response is destroying the brain, because there are
proteins that mimic the proteins in this bacteria, Acinetobacter,
which Professor Ebringer believes. So the evidence is quite compelling,
and I think it is true to say that it is not just SEAC that have
adopted this view. Professor Horn also considered this theory,
and the scientists on his Committee also thought it was not a
plausible theory, and they, as I said, are not necessarily experts
in TSEs. In addition to that, the EU Scientific Steering Committee
also considered this when they did their review of the origin,
and they are a different group of scientists, and indeed the Phillips
inquiry also came to the same view. So there are four different
groups of people who have looked at this who do not believe it
is a plausible hypothesis.
26. So in terms of decisions on funding of research
projects, for example, you have come to the conclusion that this
is a dead end as far as the discovery of the origins of BSE are
concerned?
(Dr Bailey) Yes.
Mr Todd
27. You said that very few cattle had shown
evidence of the disease before 30 months. How many have?
(Dr Bailey) I am sorry. We will have to let you have
a note on that.
28. If we take it that the 30-month rule was
devised on the basis that the disease virtually always did not
show itself until that age, we assume that the animal feed restrictions
were in place soundly as from 1 August 1996, but we have gradually
discovered that other factors must be involved in this because,
of course, animals born more than 30 months after that feed control
date have developed the disease. What explanations do we have
for that?
(Dr Nash) First of all, we have found out that there
are 81 cases in animals lower than 30 months out of 180,000.
29. That is not a particularly small amount.
But we need to put that in the context that there are some European
countries where 81 cases of any kind would be regarded as a very
large number. Can you give us a profile—you will not be
able to do it now—of when they developed the disease, whether
it was 29 months or at a much younger age?
(Dr Nash) Off the top of my head, I cannot, but we
can let you have those statistics. Turning back to your question,
first of all, before asking Peter to go into the veterinary investigations
into the cases born after 1 August 1996 and the provisional conclusions
we have reached, there are 20 such cases in the UK so far, 17
in Great Britain and three in Northern Ireland. Of the 17 in Great
Britain, roughly half have become apparent through normal surveillance
and the other half through our active testing programme. Of the
cases that have come to light as a result of the active testing
programme, all have been in the casualty cattle survey, which
is quite interesting. The other thing I should say is that Professor
Wilesmith, an epidemiologist at VLA, has been looking into the
characteristics of not the whole of the 20, because we have only
recently learned about some of them, but the first 11 GB cases,
I think it is, and is hoping to publish a short paper fairly soon
on this. All I would say at this stage is that in the case of
what we call the BAB cases, which are cases born after the original
feed ban of July 1998, the single risk factor was the ratio of
pigs and cattle. In other words, there was a strong cross-contamination.
That was the clear argument, and that seems to have been demonstrated
subsequently. In the case of at least these first 11—and,
of course, it is a very small number, so we must not be too clear
about it—there is no such link. In fact, very tentatively,
one would say that the cases are more linked to dairy cows or
to the number of cattle. There is certainly no link with the pigs.
(Mr Soul) Focusing on animals born after August 1996,
which of course was the date when we had completed our feed recall
system, and we believe it was the date from which the reinforced
feed ban should have been as secure as it has been possible to
make it, we have had this small number of cases born after that,
and of course, the big question is: where they have got the disease
from. We think there are four main possibilities: maternal transmission;
environmental contamination; horizontal transmission; and feedborne
disease, some method of continuation of the feedborne problem
that we are confident caused the former epidemic. To summarise
briefly, because of the fact that a number of dams in these cases
are still alive, we think that maternal transmission is certainly
not a likely possibility in a significant number of these cases.
It is not a common factor for all of them. It is a possibility
in a few of them, but again, only a possibility. Environmental
contamination we have looked into very thoroughly and we do not
really think there is any likelihood that that is significant,
and certainly when you look at the whole of the epidemic, it does
not seem to have featured as something which has kept the epidemic
going. Horizontal transmission—again, there are good reasons
why this does not seem very likely. A number of these cases are
the first cases on these farms, so we have had to give that a
lower consideration, which means that we come back again to foodborne
transmission. The question is: is there still some infectivity
in the system out there despite all our efforts? Is some coming
in from abroad? After all, we know that back in 1996-97 there
was infectivity circulating in Europe. There is pretty well free
trade in most commodities between Europe and us, so are we subject
to the same causes that have caused disease in France and Germany,
etc? That is a distinct possibility that we have to investigate
as thoroughly as we possibly can. Of course, it is extremely difficult;
we are going back a number of years, and to try and get evidence
of what happened in detail back then is very difficult, but those
are the areas that we are looking at.
30. Would it not be fair to say that research
into this aspect ought to be given the highest priority, examining
the outbreak and its implications? From all your answers, the
simple answer is we do not know. You have run through all of the
options, and none of them seem particularly attractive or likely
as explanations of the continuing tail of this disease in this
country.
(Mr Soul) Yes. Research is going on into some of these
areas. Environmental contamination is a possibility for example.
We have commissioned research into that, but it is hard to see
how we could construct a research project to identify what caused
the disease back in 1996. It is more a question of investigating
it.
31. But these cases are continuing to occur,
are they not, and in some cases in animals born significantly
after 1996?
(Mr Soul) Yes.
32. We are not going back into the dark ages
of time.
(Mr Soul) That is right, and we are investigating
those. Perhaps with some of the more recent ones, we stand a better
chance of making a connection. It seems quite likely that, if
what I have said is true, we will continue to get a small number
of cases until something changed, and what changed, of course,
was that a feed ban came in throughout the whole of Europe with
effect from 1 January 2001. So it may well be that we will not
see a significant change in this small number of cases, this long
tail going on, in younger animals until, say, five years after
that date.
33. Does this indicate that the 30-month rule
ought to remain in place in terms of human health protection for
quite some considerable time to come?
(Dr Nash) The Food Standards Agency is responsible
for policy on the over 30 month rule, and they have just begun
a review of the rule which is likely to conclude around the end
of the year. I would not really like to predict what that review
is going to conclude.
34. You have presumably given them some advice.
(Dr Nash) No. A key element in that review will be
the risk assessments, which have yet to be done. I think it is
very important to have thorough and independent risk assessments
to establish the actual level of risk.
35. None of you are making any submissions about
that process.
(Dr Nash) We will certainly provide information because
one of the key elements going into the risk assessments will be
the testing results. Since last July we have organised the testing
of about 220,000 animals in the UK for BSE, and there is a great
deal of information there which will certainly feed into the review.
36. Finally, the 20 cases you have identified
of animals born after August 1996—is that in line with the
expectations of those who predicted the path of this disease,
or greater than or less?
(Dr Nash) It is in line. It is a little below. The
Imperial College Group, then the Oxford Group, made forecasts
of the number of cases we should expect born after August 1996
on the assumption that there was 10 per cent maternal transmission.
37. Although we are hearing that that may well
not be the reason.
(Dr Nash) That is right. The numbers that we would
have had, had we had 10 per cent maternal transmission, would
have been slightly greater than the numbers we have actually had.
But you are perfectly right; we do not think maternal transmission
is the cause of certainly the majority of these cases, if any
of these cases.
Diana Organ
38. Are these 20 cattle that have been born
after 1 August 1996 showing the disease in the early part of their
life or are they at 27, 28, 29 months when they show it? I wonder
if you can tell me the distribution of when they are occurring
since 1996. Have they come recently, in this year, or is it because
you consider that the most likely case is from feedborne transmission?
Are they very close to and leading up to the time when there was
a feed ban across Europe? I am looking for the pattern of them
and when they are exhibiting themselves.
(Mr Soul) They are all over 30 months. That is a key
point. They are not less than 30 months when they are either going
down with the disease or where they have been found as a consequence
of the active surveillance programme.
David Taylor
39. What is the youngest age?
(Mr Soul) 31 months, a Northern Ireland case. That
is actually very interesting because that is really an outlier
in this group. It is unusual in that it seems relatively so young,
and the working assumption we would have is that it must have
had a fairly heavy exposure, presumably at a fairly young age,
to have gone down with the disease so young. The average age throughout
the whole epidemic is increasing. It was five years, it is now
more like six years, and we think that is because the exposure
that they were subject to has been declining as a consequence
of the feed bans.
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